Wednesday, July 25, 2007

Obesity and Pregnancy

Vivisectors intone an endless chant that animal models are the road to human immortality. Without such talismans, they claim, all medical research would come to a screeching halt and disease would quickly overtake us all. It is as if animals must be placed on the altar to Science and tortured to death to ward off evil spirits. People opposed to such sacrifice are Luddites or anti-human.

Any scientific-sounding question is deemed adequate to justify spending large sums of taxpayer money and hurting and killing animals. Here's a new example of meaningless research that will cost the taxpayers somewhere around $1.5 million, harm many animals, and help no one (except the University of Utah and the vivisector.)

The study is especially frivilous in light of the wealth of data pointing out the risks to human fetuses and babies when the mother is obese.

Abstract: DESCRIPTION (provided by applicant): Project summary. Accumulating evidence from our laboratory and others suggests that adult diseases originate in utero, and likely occur through the reprogramming of gene expression via epigenetic changes in chromatin structure (an altered "histone code"). Although models of intrauterine growth restriction have been established in rodent models which demonstrate that fetal alterations in the histone code are involved in the persistence and conveyance of the altered postnatal phenotype, little is known about the effects of a high fat (HF) maternal diet and resultant obesity on primate fetal biology. We hypothesized that a HF diet in non- human primates (NHP) would induce tissue specific changes in chromatin structure resulting in altered expression of fetal genes critical to the development of childhood and adult diseases. Based on (1) our preliminary data, and (2) emerging evidence that the Clock family of circadian genes functions to orchestrate multiple metabolic processes, the focus of this proposal is the epigenetic modifications in fetal circadian gene expression induced in response to a HF maternal environment. In Aim 1, we will characterize maternal HF diet-induced chromatin modifications in relevant NHP fetal tissue (hypothalamus and liver). In Aim 2, we will characterize the molecular means by which these chromatin modifications meaningfully alter fetal circadian gene expression. In Aim 3, we will determine if healthful maternal diet modification after chronic HF consumption will revert the overall pattern of the fetal histone code back to its naive state, and if diet improvement alters the epigenetic characteristics and expression of fetal genes of interest in the NHP. Relevance. Obesity causes substantial soical [sic], economic and health burdens. The rate of obesity is escalating disproportionately in children (infants to young adults). This rapid increase is unlikely to be due to environment or genetics alone. Based on previous work, we believe that obestiy in part starts when the child was a fetus in utero and occurs because of reprogramming of gene expression caused by the mother's diet and health. We will test this hypothesis in non-human primates and will determine whether improving maternal diet changes genes of interest that contribute to childhood obesity. Given the obesity epidemic, this has great public health significance.

What's the answer to the childhood obesity epidemic? Certainly not parent and child education about diet and exercise; certainly not limiting TV and video games or junk foot and pounds of sturated fat... If you believe these things might lead to some improvement, you just don't understand science.

The an$wer, of cour$e, i$ to induce obe$ity in monkey$ and then experiment on their babie$.

But the association between obese parents, particularly mothers, and later childhood obesity and its associaed problems, is already recognized. Harvard researchers Emily Oken and Matthew W. Gillman note in their review article, "Fetal Origins of Obesity" (Obesity Research, 2003), that "Maternal and paternal body habitus predict offspring fatness, particularly fatness during childhood. A combination of genetic and both pre- and postnatal environmental causes is likely. In addition, parental adiposity is directly associated with offspring birth weight, with stronger associations for the mother than for the father, which implicates prenatal environmental factors."

Interestingly, because this research will be conducted in Utah, the protocols -- the details of the study's design and how the animals will be used -- are off limits to the public. Utah has exempted all such documents from public disclosure.